Aquaporin water channels in the nervous system
By M. C. Papadopoulos, A. Verkman. Nature Reviews Neuroscience, 2013
706 citations recorded by the source corpus.
The aquaporins (AQPs) are plasma membrane water-transporting proteins. AQP4 is the principal member of this protein family in the CNS, where it is expressed in astrocytes and is involved in water movement, cell migration and neuroexcitation. AQP1 is expressed in the choroid plexus, where it facilitates cerebrospinal fluid secretion, and in dorsal root ganglion neurons, where it tunes pain perception. The AQPs are potential drug targets for several neurological conditions. Astrocytoma cells strongly express AQP4, which may facilitate their infiltration into the brain, and the neuroinflammatory disease neuromyelitis optica is caused by AQP4-specific autoantibodies that produce complement-mediated astrocytic damage.
Subfields: Molecular Biology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/e75a18f80a7bf097197ded6d14da8afe82eb84db
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Citations in the corpus
- Physiology of Astroglia. (2018, neutral): “The AQP4 is composed from eight intramembrane helical segments M1 M8 and two translation initiation sites designated as Met1 and Met23, which in turn define two AQP4 isoforms, M1 and M23 (1314).”
- Physiological roles of aquaporin-4 in brain. (2013, background): “This is not to say that AQP4 is the only aquaporin expressed in brain: AQP1, AQP9, and AQP11 also count as brain aquaporins, but these are quite restricted in their expression (AQP1, AQP9) (143) or without any clear function (AQP11) (48).”
- A new look at cerebrospinal fluid circulation (2014, background): “Currently, at least 14 different aquaporins have been identified [97,117].”
- Astrocyte roles in traumatic brain injury (2015, background): “…that many reactive astrocytes alter their expression and cellular distribution of AQP4 so as to lose their heavy polarization of AQP4 along endothelial surfaces, with consequent impact on tissue fluid homeostasis and edema formation after TBI as reviewed elsewhere (Papadopoulos and Verkman, 2013).”
- Glial Scar Borders Are Formed by Newly Proliferated, Elongated Astrocytes That Interact to Corral Inflammatory and Fibrotic Cells via STAT3-Dependent Mechanisms after Spinal Cord Injury (2013, background): “4A; Papadopoulos and Verkman, 2013).”